Gpr43 regulates sodium butyrate-induced angiogenesis and matrix remodeling.

GPR43 REGULATES SODIUM BUTYRATE-INDUCED ANGIOGENESIS AND MATRIX REMODELING. Am J Physiol Heart Circ Physiol. 2020 Dec 24;: Authors: Castro PR, Bittencourt LFF, Larochelle S, Andrade SP, Mackay CR, Slevin MA, Moulin VJ, Barcelos LS Abstract Butyrate is a short-chain fatty acid (SCFA) derived from microbiota and is involved in a range of cell processes in a concentration-dependent manner. Low concentrations of sodium butyrate (NaBu) was shown to be proangiogenic. However, the mechanisms associated with these effects are not yet fully known. Here, we investigated the contribution of the SCFA receptor GPR43 in the proangiogenic effects of local treatment with NaBu and its effects on matrix remodeling using the sponge-induced fibrovascular tissue model in mice lacking the GPR43 gene (GPR43-KO) and the wild-type (WT). We demonstrated that NaBu (0.2 mM intraimplant) treatment enhanced the neovascularization process, blood flow, and VEGF levels in a GPR43-dependent manner in the implants. Moreover, NaBu was able to modulate matrix remodeling aspects of the granulation tissue such as proteoglycans production, collagen deposition and α-SMA expression in vivo, besides to increase TGF-b1 levels in the fibrovascular tissue, in a GPR43-dependent manner. Interestingly, NaBu directly stimulated L929 murine fibroblasts migration, and TGF-β1 and collagen production in vitro. GPR43 was found to be expressed in human dermal fibroblasts, myofibroblasts...
Source: American Journal of Physiology. Heart and Circulatory Physiology - Category: Physiology Authors: Tags: Am J Physiol Heart Circ Physiol Source Type: research